the respiratory system part 2
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The Respiratory System Part 2
The Respiratory CycleA respiratory cycle is a single cycle of inhalation and exhalation. The tidal volume is the amount
of air you move into or out of your lungs during a single respiratory cycle.
The Mechanics of Breathing
The Respiratory Muscles
The most important are the diaphragm and the external intercostal muscles .
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Muscles sed in !nhalation
!nhalation is an active process involving the contraction of one or more of these muscles"
The contraction of the diaphragm increases the volume of the thoracic cavity #y tensing and
flatteningits floor$ and this increase dra%s air into the lungs. &iaphragmatic contraction isresponsi#le for roughly 75 percentof the air movement in normal #reathing at rest.
The external intercostal muscles assist in inhalation #y elevating the ribs. This action
contri#utes roughly 2' percent to the volume of air in the lungs.
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Accessory muscles$ including the sternocleidomastoid$ serratus anterior$ pectoralis minor$ and
scalene muscles$ can assist the external intercostal muscles in elevating the ri#s. These musclesincrease the speed and amount of ri# movement.
Muscles sed in (xhalation
(xhalation is either passive or active$ depending on the level of respiratory activity. )hen
exhalation is active$ it may involve one or more of the follo%ing muscles"
The internal intercostal and transversus thoracis muscles depress the ri#s and reduce the %idth
and depth of the thoracic cavity.
The a#dominal muscles$ including the external and internal o#li*ue$ transversus a#dominis$ and
rectus a#dominis muscles$ can assist the internal intercostal muscles in exhalation #ycompressing the a#domen and forcing the diaphragm up%ard.
Respiratory Rates and +olumes
)hen you are exercising at pea, levels$ the amount of air moving into and out of the respiratory
tract can #e 50 times the amount moved at rest.
Respiratory Rate is the num#er of #reaths you ta,e each minute. The normal respiratory rate of a
resting adult ranges from -2 to - #reaths each minute$ roughly one for every four heart#eats.
Children #reathe more rapidly$ at rates of a#out -/20 #reaths per minute.
The Respiratory Minute +olume is the amount of air moved each minute$ sym#oli1ed #y
multiplying the respiratory rate #y the tidal volume. This value is called the respiratory minute
volume . The tidal volume at rest varies from individual to individual$ #ut it averages around 500
ml per breath.Therefore$ the respiratory minute volume at rest$ -2 #reaths per minute$ is
approximately liters per minute.
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Alveolar +entilation
The volume of air in the conducting passagesis ,no%n as the anatomic dead space.
Alveolar ventilation is the amount of air reaching the alveoli each minute. The alveolarventilation is less than the respiratory minute volume$ #ecause some of the air never reaches the
alveoli$ #ut remains in the dead space of the lungs.
At rest$ alveolar ventilation rates are approximately 3.2 liters per minute The gas arriving in thealveoli is different from that of the surrounding atmosphere$ #ecause inhaled air al%ays mixes
%ith "used"air in the conducting passage%ays 4the anatomic dead space5 on its %ay to the
exchange surfaces. The air in alveoli thus contains less oxygen and more car#on dioxide thanatmospheric air.
Respiratory Performance and +olume Relationships
Only a small proportion of the air in the lungs is exchanged during a single quiet respiratory
cycle6 the tidal volume can #e increased #y inhaling more vigorously and exhaling more
completely.
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t
Respiratory +olumes and Capacities.
The resting tidal volume is the amount of air you move into or out of your lungs during a singlerespiratory cycle under resting conditions. The resting tidal volume averages a#out '00 ml in
#oth males and females.
The expiratory reserve volume 4(R+5 is the amount of air that you can voluntarily expelafter
you have completed a normal$ *uiet respiratory cycle. As an example$ if$ %ith maximum use of
the accessory muscles$ you can expel an additional -000 ml of air$ your expiratory reservevolume is -000 ml.
The residual volume is the amount of air that remains in your lungs even aftera maximal
exhalation/typically$ a#out -200 ml in males and --00 ml in females.
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The minimal volume $ a component of the residual volume$ is the amount of air that %ould
remain in your lungs if they %ere allo%ed to collapse. The minimal volume ranges from 70 to
-20 ml$ #ut$ unli,e other volumes$ it cannot #e measured in a healthy person. 8ou %ould have tos*uee1e out the lungs li,e a sponge to measure it.
The inspiratory reserve volume 4!R+5 is the amount of air that you can ta,e in over and a#ove
the tidal volume. !nspiratory reserve volumes differ significantly #y gender$ #ecause$ on average$the lungs of males are larger than those of females. The inspiratory reserve volume of males
averages 7700 ml$ compared %ith -900 ml in females.
)e can determine respiratory capacities #y adding the values of various volumes. (xamples
include the follo%ing"
The inspiratory capacity is the amount of air that you can dra% into your lungs after you have
completed a *uiet respiratory cycle. The inspiratory capacity is the sum of the tidal volume and
the inspiratory reserve volume.
The functional residual capacity 4:RC5 is the amount of air remaining in your lungs after you
have completed a *uiet respiratory cycle. The :RC is the sum of the expiratory reserve volume
and the residual volume.
The vital capacity is the maximum amount of air that you can move into or out of your lungs in a
single respiratory cycle. The vital capacity is the sum of the expiratory reserve$ the tidal volume$
and the inspiratory reserve and averages around 300 ml in males and 7300 ml in females.
The total lung capacity is the total volume of your lungs. The sum of the vital capacity and the
residual volume$ the total lung capacity averages around 000 ml in males and 3'00 ml infemales.
;as (xchange
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The actual process of gas exchange occurs #et%een #lood and alveolar air across the respiratory
mem#rane. !t involves" 4-5 the partial pressures of the gases involved and 425 the diffusion of
molecules #et%een a gas and a li*uid.
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The attachment of the first oxygen molecule ma,es it easier to #ind the second6 #inding the
second promotes #inding of the third6 and #inding of the third enhances #inding of the fourth$
and so on.
At normal alveolar pressures the hemoglo#in saturation is very high 49>.' percent5$ although
complete saturation does not occur until the reaches excessively high levels 4a#out 2'0 mm =g5.
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!f the P?
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)hen the pH drops (more acidity)$ the shape of hemoglo#in molecules changes6 the oxygensaturation declines. Thus$ at a tissue of 30 mm =g$ hemoglo#in molecules release -' percent
more oxygen at a p= of >.2 than they do at a p= of >.3. This effect of p= on the hemoglo#insaturation curve is called the Bohr effect .
arbon dioxide is the primary compoundresponsi#le for the Bohr effect.
The (ffects of p= and Temperature on =emoglo#in Saturation.
4a5 )hen the p= drops #elo% normal levels$ more oxygen is released6 the hemoglo#in
saturation curve shifts to the right. !f the p= increases$ less oxygen is released6 the curve shifts to
the left. 4#5 )hen the temperature rises$ the saturation curve shifts to the right
=emoglo#in and Temperature
Changes in temperature also affect the slope of the hemoglo#in saturation curve . As the
temperature rises$ hemoglo#in releases more oxygen6 as the temperature declines$ hemoglo#in
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Atmospheric pressure decreases %ith increasing altitude$ and so do the partial pressures of the
component gases$ including oxygen. People living in &enver or Mexico City function normally%ith alveolar oxygen pressures in the range of 0/90 mm =g. At higher elevations$ the alveolar
partial pressures of oxygen continues to decline. At 7700 meters 4-0$2 ft5$ an altitude familiarto many hi,ers and s,iers$ the alveolar P?
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The #icar#onate ions move into the surrounding plasma %ith the aid of a countertransport
mechanism that exchanges intracellular #icar#onate ions for extracellular chloride ions. Thisexchange$ %hich trades one anion for another$ does not re*uire ATP. The result is a mass
movement of chloride ions into the RBCs$ an event ,no%n as the chloride shift .
=emoglo#in Binding
Roughly 27 percent of the car#on dioxide carried #y your #lood %ill #e #ound to the glo#ularprotein portions of the =# molecules inside RBCs. These molecules are attached to exposed
amino groups of the =# molecules. The resulting compound is called car#aminohemoglo#in
Plasma TransportPlasma #ecomes saturated %ith car#on dioxide *uite rapidly$ and only a#out > percent of the
car#on dioxide a#sor#ed #y peripheral capillaries is transported in the form of dissolved gas
molecules.
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Control of Respiration
The activities of the respiratory centers are coordinated with changes in cardiovascular
function" such as fluctuations in blood pressure and cardiac output.
ocal Regulation of ;as Transport and Alveolar :unction
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ocal factors coordinate 4-5 lung perfusion $ or #lood flo% to the alveoli$ %ith 425 alveolar
ventilation $ or airflo%$ over a %ide range of conditions and activity levels.
As #lood flo%s toward the alveolar capillaries$ it is directed to%ard lo#ules in %hich the P?C
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After 2 seconds$ the &R; neurons #ecome inactive. They remain *uiet for the next 7 seconds
and allo% the inspiratory muscles to relax.
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Central nervous system stimulants$ such as cocaine" amphetamines" ecstacy" or even caffeine$
increase your respiratory rate #y facilitating the respiratory centers. These actions can #e
opposed #y CS depressants$ such as ethyl alcohol" barbiturates or opiates. A mixture of thesestimulants and depressants is often fatal.
The Apneustic and Pneumotaxic Centers
The apneustic centers and the pneumotaxic centers of the ponsare paired nuclei that ad@ust theoutput of the respiratory rhythmicity centers. Their activities regulate the respiratory rateand the
depthof respiration in response to sensory stimuli or input from other centers in the #rain.
(ach apneustic center provides continuous stimulation to the &R; on that side of the #rain stem.
&uring *uiet #reathing$ stimulation from the apneustic center helps increase the intensity of
inhalation over the next 2 seconds. nder normal conditions$ after 2 seconds the apneustic centeris inhi#ited #y signals from the pneumotaxic center on that side. &uring forced #reathing$ the
apneustic centers also respond to sensory input from the vagus nerves regarding the amount oflung inflation.
The pneumotaxic centers inhi#it the apneustic centers and promote passive or active exhalation.
Centers in the hypothalamus and cere#rum can alter the activity of the pneumotaxic centers$ as%ell as the respiratory rate and depth. =o%ever$ essentially normal respiratory cycles continue
even if the #rain stem superior to the pons has #een severely damaged. !f the inhi#itory output of
the pneumotaxic centers is cut off #y a stro,e or other damage to the brain stem$ and if
sensory innervation from the lungs is eliminated #y cutting the vagus nerves$ the person inhalesto maximum capacity and maintains that state for 10-&0 seconds at a time. nterveningexhalations are brief" and little pulmonary ventilation occurs.
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Pathways for conscious control over respiratory muscles are not shown.
Respiratory Reflexes
The activities of the respiratory centers are modified #y sensory information from severalsources"
-. Chemoreceptors sensitive to the p=$ or of the #lood or cere#rospinal fluid.
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2. Changes in #lood pressure in the aortic or carotid sinuses.
7. Stretch receptors that respond to changes in the volume of the lungs.
3. !rritating physical or chemical stimuli in the nasal cavity$ larynx$ or #ronchial tree.
'. seconds5.Most cri# deaths occur #et%een midnight and 9"00 A.M.$ in the late fall or %inter$ and involve
infants t%o to four months old.
The age at the time of death corresponds%ith a period %hen the pacema,er complex andrespiratory centers are establishing connections with other portions of the brain. !t has
recently #een proposed that S!&S results from a pro#lem in the interconnection process thatdisrupts the reflexive respiratory pattern.
The Chemoreceptor Reflexes
The respiratory centers are strongly influenced #y chemoreceptor inputs from cranial nerves !Eand E and from receptors that monitor the composition of the cere#rospinal fluid 4CS:5"
Chemoreceptors are located on the ventrolateral surface of the medulla o#longata in a region
,no%n as the chemosensitive area . The neurons in that area respond only to the and p= of the
CS: and are often called central chemoreceptors .
The Baroreceptor Reflexes
)e descri#ed the effects of carotid and aortic #aroreceptor stimulation on systemic #lood
pressure in Chapter 2- . The output from these #aroreceptors also affects the respiratory centers.)hen #lood pressure falls$ the respiratory rate increases6 %hen #lood pressure rises$ the
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respiratory rate declines. This ad@ustment results from the stimulation or inhi#ition of the
respiratory centers #y sensory fi#ers in the glossopharyngeal 4!E5 and vagus 4E5 nerves.
Protective Reflexes operate %hen you are exposed to toxic vapors$ chemical irritants$ ormechanical stimulation of the respiratory tract. The receptors involved are located in the
epithelium of the respiratory tract. (xamples of protective reflexes include snee1ing$ coughing$
and laryngeal spasms.
Snee1ing is triggered #y an irritation of the %all of your nasal cavity. Coughing is triggered #y an
irritation of your larynx$ trachea$ or #ronchi. Both reflexes involve apnea$ a period in %hichrespiration is suspended. They are usually follo%ed #y a forceful expulsion of air intended to
remove the offending stimulus. The glottis is forci#ly closed %hile the lungs are still relatively
full. The a#dominal and internal intercostal muscles then contract suddenly$ creating pressuresthat %ill #last air out of your respiratory passage%ays %hen the glottis reopens. !ir leaving the
larynx can travel at 160 ph ! mph#" carrying mucus" foreign particles" and irritating
gases out of the respiratory tract via the nose or mouth.
aryngeal spasms result from the entry of chemical irritants$ foreign o#@ects$ or fluids into the
area around the glottis. This reflex generally closes your air%ay temporarily. A very strongstimulus$ such as a toxic gas$ could close the glottis so po%erfully that you could lose
consciousness and die %ithout ta,ing another #reath. :ine chic,en #ones or fish #ones that pierce
the laryngeal %alls can also stimulate laryngeal spasms$ s%elling$ or #oth$ restricting the air%ay.
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Both fever and an increase in #ody temperature due to exertion or overheating cause an increase
in the respiratory rate. A reduction in #ody temperature leads to a decrease in the respiratory rate.
Curiously$ stretching the anal sphincter stimulates the respiratory centers and increases the rateof respiration. Although this reflex is occasionally used to stimulate respiration in an emergency$
it is not clear %hich path%ays are involved.$nough said a%out that&
+oluntary Control of RespirationActivity of your cere#ral cortex has an indirect effect on your respiratory centers$ as the
follo%ing examples sho%"
Conscious thought processes tied to strong emotions$ such as rage or fear$ affect the respiratory
rate #y stimulating centers in the hypothalamus.
(motional states can affect respiration through the activation of the sympathetic or
parasympathetic division of the autonomic nervous system. Sympathetic activation causes
#ronchodilation and increases the respiratory rate6 parasympathetic stimulation has the oppositeeffect.
An anticipation of strenuous exercise can trigger an automatic increase in the respiratory rate$
along %ith increased cardiac output$ #y sympathetic stimulation.
8ou cannot ,ill yourself #y holding your #reath Ftill you turn #lue.F
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placental connection is lost$ #lood oxygen levels fall and car#on dioxide levels clim# rapidly. At
#irth$ the ne%#orn infant ta,es a truly heroic first #reath through po%erful contractions of the
diaphragmatic and external intercostal muscles.
The changes in #lood flo% that occur lead to the closure of the foramen ovale $ an interatrial
connection$ and the ductus arteriosus $ the fetal connection #et%een the pulmonary trun, and the
aorta.
Su#se*uent #reaths complete the inflation of the alveoli.
Aging and The Respiratory System
Many factors interact to reduce the efficiency of the respiratory system in elderly individuals.
Three examples are particularly note%orthy"
As ones age increases$ elastic tissue deteriorates throughout the body$ reducing the
compliance of the lungs and lo%ering their vital capacity.
Chest movements are restricted by arthritic changes in the rib articulations and by
decreased flexibility at the costal cartilages.The stiffening and reduction in chest movement
effectively limit the respiratory minute volume. This restriction contri#utes to the reduction in
exercise performance and capa#ilities %ith increasing age.
Some degree of emphysema is normal in individuals over age '0. =o%ever$ the extent varies
%idely %ith the lifetime exposure to cigarette smo,e and other respiratory irritants.
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/mphysema $ ung ancer
(mphysema is a chronic$ progressive condition characteri1ed #y shortness of #reath and an
ina#ility to tolerate physical exertion. The underlying pro#lem is the destruction of alveolar
surfaces and inadequate surface area for oxygen and car%on dioxide exchange . !n essence$respiratory #ronchioles and alveoli are functionally eliminated.
(mphysema has #een lin,ed to the inhalation of air that contains fine particulate matteror
toxic vapors$ such as those in cigarette smo,e.
An estimated percent of adult males and 2' percent of adult females have detecta#le areas of
emphysema in their lungs.
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ung cancer is an aggressive class of malignancies originating in the bronchial passageways oralveoli. These cancers affect the epithelial cells that line conducting passage%ays$ mucous
glands$ or alveoli. Symptoms generally do not appear until the condition has progressed to thepoint at %hich the tumor masses are restricting airflo% or compressing ad@acent structures
&eaths from lung cancer %ere rare at the turn of the 20th century$ #ut 29$000 such deaths
occurred in -9'$ -0'$000 in -9>$ and -'3$900 in 2002 in the nited States. This rise coincides%ith an increased rate of smo,ing in the population.
ung cancer is increasing mar,edly among %omen$ #ut declining among men.
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